This study is designed to examine the role of adrenal androgen excess in the pathogenesis of idiopathic hirsutism, hirsutism plus amenorrhea, and amenorrhea alone. The plasma steroid profile (including testosterone, androstenedione, dehydroepiandrosterone (DHEA), and DHEA-sulfate, LH, FSH and prolactin blood levels were measured basally and in response to stimulation with ACTH and metyrapone, LH-RH and TRH and to suppression (1-dopa), prior to and following 3 months of treatment with dexamethasone (DEX) 0.5 mg, at night in patients and in normal women (follicular phase of menstrual cycle). Prior to DEX androgen levels were significantly elevated in the patients but showed normal incremental responses to stimulation; the LH response to LH-RH was exaggerated in patients and prolactin levels were elevated and several patients showed abnormal responses to stimulation and/or suppression. Following DEX androgen levels in patients fell into or below the normal range, the androgen response to stimulation was markedly suppressed (little change in glucocorticoid response) and abnormalities in LH and prolactin secretion were unchanged. Hirsutism improved in 60% of patients, and all patients with menstrual disturbances, other than those with weight loss associated amenorrhea, resumed regular ovulation during DEX. These preliminary results suggest that adrenal androgen excess is at least in part responsible for the clinical disorders but that associated disorders in LH and prolactin are not corrected by returning androgen levels to normal. Examination of the steroid profile in patients failed to reveal evidence of an enzyme defect and the response to stimulation was normal suggesting excessive stimulation rather than an intrinsic adrenal abnormality. Isolated androgen suppression suggests the existance of a non-ACTH factor responsible for adrenal androgen secretion which may be produced in excess in many hirsute and/or amenorrheic patients.